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Macrophage colony stimulating factor prevents NMDA‐induced neuronal death in hippocampal organotypic cultures
Author(s) -
Vincent Valerie A. M.,
Robinson Christopher C.,
Simsek Dilek,
Murphy Greer M.
Publication year - 2002
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.2002.01087.x
Subject(s) - neuroprotection , excitotoxicity , hippocampal formation , nmda receptor , neuroscience , caspase , biology , programmed cell death , apoptosis , macrophage colony stimulating factor , receptor , macrophage , biochemistry , in vitro
Macrophage colony stimulating factor (M‐CSF) and its receptor are up‐regulated in the brain in Alzheimer's disease (AD), in transgenic mouse models for AD, and experimental models for traumatic and ischemic brain injury. M‐CSF induces activation and proliferation of microglial cells and expression of proinflammatory cytokines. We examined the role of M‐CSF in excitotoxic neuronal cell death in organotypic hippocampal cultures. NMDA treatment induced neuronal apoptosis and caspase‐3 activation in organotypic hippocampal cultures, whereas treatment with M‐CSF protected hippocampal neurons from NMDA‐induced apoptosis. Caspase‐3 activation was inhibited by M‐CSF treatment to the same degree as with the caspase inhibitor Z‐VAD‐FMK. These results suggest that M‐CSF has neuroprotective properties through inhibition of caspase‐3 that could promote neuronal survival after excitotoxic insult. The role of M‐CSF in neurological disease should be reevaluated as a microglial activator with potentially neuroprotective effects.